What's Hot

What's Hot

November 2003

What's Hot Archive

November 26, 2003

Fiber may mediate relationship between diet and inflammation

A reportring in the December 2003 issue of The American Journal of Cardiology established an association between fiber consumption and reduced levels of C-reactive protein (CRP), a marker of inflammation that has, when elevated, been linked with cardiovascular disease. The study also found a modest positive association between the intake of saturated fat and CRP levels.

Information the gathered from the 1999 to 2000 National Health and Nutrition Examination Survey (NHANES) was analyzed by the researchers for the current report. There were 4900 adults whose CRP levels were available from the NHANES population database. The intake of various nutrients was calculated from reports provided by participants of foods consumed on a given day. Data on the daily consumption of fiber, total fat, saturated fatty acids, monounsaturated fatty acids, polyunsaturated fatty acids, protein, carbohydrates, total calories and cholesterol was provided. Demographic variables such as age and gender and factors such as smoking and alcohol consumption were also included in the analysis.

When fiber was examined, participants whose consumption of fiber was in the top 50 percent had a significantly lower risk of elevated CRP than the remaining half, with those in the top one-fourth having a 23% lower median CRP than individuals in the lowest quarter of fiber intake. Saturated fat consumption was associated with an increase in CRP.

Previous studies have provided some findings concerning diet and inflammatory markers yet much research needs to be done in this area. The authors propose further studies uti liz ing high fiber diets or supplements to provide more information on fiber's protective mechanism against the inflammation associated with cardiovascular disease.

—D Dye

November 21, 2003

Ginseng reduces oxidative stress associated with aging in rats

The November 2003 issue of the Journal of Nutrition reported the findings of researchers from the University of Wisconsin that ginseng protects against oxidative stress in aging rodents. Oxidative stress occurs when dangerous molecules known as free radicals overwhelm the body's antioxidant defense system and cause oxidative damage to lipids, proteins, DNA and other molecules.

The researchers divided four month old and twenty-two month old female rats into three groups who were fed a diet supplemented with a low dose of powdered North American ginseng, a high dose of the herb, or no ginseng. When oxidant generation was measured in tissue samples from three different locations, it was found to be lower in both the young and old rats who received ginseng, with those who received the greater dose having experienced the least amount of oxidative stress. Superoxide dismutase , one of the antioxidants made in the body, was elevated in the heart and deep portion of the vastus lateralis muscle of rats who received the higher dose of ginseng. Another endogenous antioxidant, glutathione peroxidase , was elevated in the vastus lateralis and soleus muscles of this group. When lipid peroxidation (an indicator of oxidative damage to cellular lipids) was measured, there was no benefit observed in the rats who received ginseng, but protein carbonyl content, a measurement of protein oxidation, was improved in the heart and vastus lateralis muscle of those who received the greater dose.

Thus it was concluded that ginseng prevents the age-associated increase in oxidant production in rats as well as oxidative protein damage. Prior research on ginseng has utiliz ed Asian varieties, while this study demonstrated the benefits of North American ginseng. Although earlier studies had revealed ginseng's free radical scavenging ability in vitro, this investigation is the first to confirm this benefit in a living model.

—D Dye

November 19, 2003

Inflammation is culprit in yet another condition

In the November 2003 issue of The Journal of Vascular Surgery , researchers funded in part by the National Institutes of Health reported that deep vein thromboses (DVT: blood clots that form in the legs) may be caused by an inflammatory process, similar to the blockage that occurs in the arteries in atherosclerosis. The condition was previously believed to be a vascular or blood disorder.

In the current study, the University of Michigan Medical School team induced blood clots in 659 mice consisting of one group bred to have high levels of P- selectin , a second group lacking the P- selectin gene, a third group lacking P- selectin as well as the related E- selectin , and a control group of normal mice. P- selectin , a pro-inflammatory molecule, has been found to be expressed in the vein wall after a blood clot begins to form. The researchers found that mice with the highest levels of blood P- selectin developed the largest clots and had a greater number of inflammatory cells in the walls of their veins. These mice were also found to have microparticles in their blood consisting of cell membranes from degraded white blood cells, blood platelets or vessel wall endothelial cells.

Coauthor and assistant professor of vascular surgery and animal medicine at the University of Michigan Medical School, Daniel D. Myers, DVM, announced, “ Our laboratory is the first to evaluate microparticle formation in a mouse model of DVT. We found that when P- selectin binds to its receptor, it seems to release these procoagulant microparticles, which accelerate the clot-forming process. Mice with more leukocyte-derived microparticles developed larger blood clots than mice with microparticles derived primarily from blood platelets."

Colleague Thomas W. Wakefield , MD, added, “Just stopping inflammation alone will not inhibit thrombosis. You have to target the interaction between inflammation and thrombosis, which is why we think P- selectin or leukocyte-derived microparticles would make good therapeutic targets."

—D Dye

November 17, 2003

Lycopene inhibits growth of normal prostate cells

The dietary carotenoid lycopene has been demonstrated in several studies to be associated with a reduction in prostate cancer cell growth. In the first study to test the effects of lycopene on noncancerous cells, researchers from the University of California at Davis found that lycopene has an inhibitory effect on the growth of normal prostate epithelial cells in vitro, leading them to speculate that the compound could have preventive or therapeutic benefits in benign prostate hyperplasia ( enlargement of the prostate gland) which frequently occurs in older men and can sometimes precede the development of prostate cancer. The report appeared in the November 2003 Journal of Nutrition .

The researchers used cultures of normal prostate epithelial cells to which was added a solution of varying concentrations synthetic lycopene . Control cell cultures received the solution without lycopene or no treatment. Lycopene was found to significantly and dose-dependently inhibit the growth of the prostate epithelial cells in concentrations of 1 micromole per liter or greater. At 2 micromoles per liter concentration, an approximate 80 percent inhibition of prostate epithelial cell growth was achieved. This amount of inhibition is greater than that previously reported for lycopene when tested on prostate cancer cells. While studies have found a 20 to 25 percent inhibition in growth on several prostate cancer cell lines using 5 micromoles per liter of lycopene , the current study found a 20 percent reduction in normal cells at only 0.3 micromoles per liter.

Lycopene is one of the carotenoid compounds that preferably accumulates in the human prostate. If lycopene inhibits prostate cell growth in vitro it is reasonable to anticipate that it may also be found to do so in the body. By inhibiting normal prostate cell proliferation, lycopene consumption could reduce the risk of developing prostate cancer.

—D Dye

November 14, 2003

Anti-inflammatory agents key to healing brain

In an advance online publication of the December 5 2003 print edition of the journal Science, researchers from Stanford University School of Medicine have found that inflammation may be responsible for the brain's lack of ability to heal from damage, and that anti-inflammatory drugs related to ibuprofen may recover some of this ability.

It had been observed that individuals who received radiation to destroy brain tumors experienced damage to healthy brain cells, especially those in the hippocampus, the brain's memory center. In an attempt to improve the resultant memory loss and learning deficits, researchers tried implanting brain stem cells to replace lost neurons, but found them to be ineffective. First author Michelle Monje explained, "They are still there, but they can't do their job. Something was wrong in the environment where the stem cells should be making neurons."

Monje and colleagues suspected that the inflammatory cells that migrated to the damaged area could be responsible for the problem, and tested the idea on rats who received an inflammatory substance which caused them to lose neurons. They then injected the rats with a nonsteroidal anti-inflammatory drug (NSAID) and found that in one week the stem cells were creating neurons at the same rate as in rats who did not receive the inflammatory substance. In another experiment in which the animals received a drug that blocked the action of interleukin-6, rats who received the inflammatory substance were able to form normal neuronal cells from stem cells. And in a final experiment, the researchers found that NSAIDs given after exposure to radiation allowed those who received the drug to create more new hippocampal neurons than those who did not receive it.

Monje predicted, "This work may open up therapeutic avenues for people who need radiation treatment."

—D Dye

November 12, 2003

Ginkgo improves verbal recall

The Society for Neuroscience's annual meeting, that was held from November 8 through November 12 2003 in New Orleans , was the site of the presentation of findings from the UCLA Neuropsychiatric Institute that the herb ginkgo biloba taken for six months improved recall in individuals with age-associated memory impairment.

The study included ten individuals between the ages of 45 and 75 who complained of mild memory loss who were provided with 120 milligrams ginkgo biloba or a placebo twice daily. The researchers used positron-emission tomography (PET) to measure brain metabolism and cognitive tests to measure recall before and after the treatment period.

After six months, all of the participants who received ginkgo experienced an improvement in verbal recall. Although improved recall correlated with better function in brain memory centers, the PET scans did not find a difference in brain metabolism between the treatment and placebo groups, possibly due to the small sample size. Lead author and assistant clinical professor at the UCLA Neuropsychiatric Institute, Dr Linda Ercoli, commented, "Our findings suggest intriguing avenues for future study, including using PET with a larger sample to better measure and understand the impact of gingko biloba on brain metabolism. “

Previous studies on ginkgo have provided conflicting results concerning its benefit on memory loss. This study is the first to measure the effect of ginkgo biloba taken over a longer period of time. Principle investigator and director of the Aging and Memory Research Center at the UCLA Neuropsychiatric Institute, Dr Gary Small, added, “The research also raises questions regarding the significance of supplement quality and treatment duration. The Food and Drug Administration does not regulate dietary supplements, and the quality of retail supplies varies widely. We used only the highest grade of ginkgo biloba in conducting our research."

—D Dye

November 10, 2003

Green tea compound prevents HIV from binding to T cells

The November 2003 issue Journal of Allergy and Clinical Immunology published the findings of Kuzushige Kawai, MD, and colleagues from the University of Tokyo that epigallocatechin gallate (EGCG), a green tea catechin found to be responsible for many of the drink's health benefits, prevents the binding of HIV to human T cells, which is the initiation step in becoming infected with HIV. The description of EGCG's mechanism in blocking HIV is the first of its kind to be published.

The researchers discovered that EGCG prevented the envelope glycoprotein of the human immunodeficiency virus from binding to CD4 molecules located on human T cells, which are the immune cells that are attacked by HIV. In an accompanying editorial in the same issue of the journal, William T. Shearer, MD, PhD and colleagues from Baylor College of Medicine in Houston , Texas report on their use of computer programs to help define the nature of these effects. Dr Shearer stated, "It might be possible to locate the precise EGCG binding spot on the CD4 molecule and compare that spot to where the HIV glycoprotein normally binds, in an attempt to explain the exciting discovery of Dr. Kawai. Molecular modeling of a drug form of EGCG for HIV infection might be a further development of these investigations."

Green tea polyphenols have been demonstrated to provide many health benefits, such as the scavenging of free radicals and protection against cancer and heart disease. The concentrations of EGCG used in this study were are many times greater than what could be achieved by drinking green tea in normal amounts, but ECGC as an isolated agent may prove to be an effective drug in the battle against HIV infection.

—D Dye

November 7, 2003

Duke University doctors propose health care overhaul

Two physicians from Duke University have condemned the American health care system as inefficient, expensive, wasteful and frequently inaccessible, yet they offer a solution that calls for a new direction in health care. In an article published in the November issue of Academic Medicine , President and CEO of the Duke University Health System, Ralph Synderman , MD , and Sanders Williams MD, Dean of Duke University School of Medicine propose a plan that involves applying the latest scientific knowledge and tools to prevent or minimize disease rather than treat it.

Dr Snyderman commented, “Emerging scientific fields -- including genomics, proteomics, metabolomics and diagnostic imaging -- can facilitate assessment of each individual's risk for developing disease, as well as early diagnosis and effective prevention and treatment. This is particularly important for the major chronic diseases, such as cancer, cardiovascular disease, diabetes, asthma and musculoskeletal disorders, which account for the greatest burden of human suffering. Yet despite vast expenditures for health care, 40 million Americans today lack ready access to health services and effective therapies are inconsistently and ineffectively applied."

The Duke leaders call for a prospective health care model in which physicians could make use of the new tools available to determine disease risk, enabling them to plan preventive interventions and watch for the development of diseases in their early stages when treatment is more effective. Healthcare coaches would assist patients in implementing customized plans into their personal routines,

Without such a shift in practice, the authors warn, increasing medical costs will only continue to provide inefficient treatment. Duke University has already begun to implement the physicians' recommendation by collaborating with the Center for the Advancement of Genomics to create the first comprehensive practice of genomic based prospective medicine.

—D Dye

November 5, 2003

Multivitamin supplementation lowers LDL cholesterol oxidation and homocysteine

The October 2003 issue of the Journal of the American College of Nutrition published the results of a double-blinded placebo controlled study that reveal the protective benefit of multivitamin supplementation against coronary heart disease. The trial sought to verify preliminary data discovered in a pilot trial published in Applied Nutritional Investigation in 2002.

Researchers from the Cooper Institute for Aerobics Research in Dallas, Texas, in conjunction with Tufts University and the University of Texas Southwest Medical Center randomized 182 participants to receive a twenty-four ingredient multinutrient supplement or a placebo, and measured homocysteine , lipids, and low density lipoprotein (LDL) cholesterol oxidation as well as levels of several vitamins at the study's onset and at six months.

While vitamin levels predictably rose in the supplemented group, homocysteine and LDL oxidation were more greatly reduced than in the placebo group, with decreases of 17 and 14 percent, respectively. At the same time, the LDL oxidation rate declined and lag time (resistance to oxidation) increased in the supplemented group.

Elevations in both homocysteine levels and LDL cholesterol oxidation are risk factors for coronary heart disease. The amino acid homocysteine , dubbed “the cholesterol of the 21 st century, has been found in several studies to be associated with the early development of cardiovascular disease, and is also associated with deficiencies of folic acid, vitamin B6 and B12. LDL cholesterol, when oxidized, is more likely to adhere to arterial walls leading to increased plaque formation, and antioxidant vitamins may help to prevent this. Reductions in these two risk factors may help protect against heart attacks and other cardiovascular events.

—D Dye

November 3, 2003

High dose thiamine helps prevent diabetic kidney troubles

The August 2003 issue of the journal Diabetes published the findings of researchers from the University of Essex in England that high doses of thiamine, also known as vitamin B1, helps prevent renal (kidney) disease in diabetic rats. Renal disease is an unfortunate result of diabetes in many patients with the condition (known as diabetic nephropathy) that has a high rate of cardiovascular complications in its end stages. Individuals who have achieved tight glucose control with insulin therapy are still at risk for developing diabetic nephropathy.

The research team induced diabetes in rats who were then provided with 7 or 70 milligrams per kilogram body weight thiamine, or benfotiamine, the fat soluble version of the vitamin, for a twenty-four week period. Control groups of rats received similar regimens. Thiamine intake in the various treatment groups exceeded the recommended daily allowance from 20 to 140 fold.

Diabetic rats were placed on moderate insulin therapy. It was found that thiamine and benfotiamine inhibited the development of microalbuminuria, a sign of renal disease, by 70 to 80 percent compared to controls, without a dose dependent relationship observed. This was associated with a reduction in protein kinase C activation, protein glycation and oxidative stress, which are pathways of biochemical dysfunction in states of elevated blood glucose. When protein in the urine, another sign of renal disease, was analyzed, the vitamins showed a similar protective effect, with a dose dependent effect for thiamine but not benfotiamine .

The researchers discovered that the diabetic rats in this study had an increase in thiamine excretion compared to controls, rendering them deficient in the vitamin. They proposed that, “clinical diabetic subjects should avoid becoming thiamine deficient, even weakly so, and that high-dose thiamine repletion should be considered for therapy to prevent the development of clinical diabetic nephropathy.” ( Babai-Jadidi R et al, “Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine ,” Diabetes vol 52, August 2003, p 2110-2120.)

—D Dye

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